The
dumping of PCBs in large bodies of water such as lakes and rivers was banned in
the United States in 1977 [3]. Before its banning, the dumping of such toxic
chemicals was overwhelming common as their use was prominent in the manufacturing
sector [3]. In the Hudson River alone, over a million pounds of PCBs were
released by General Electric during the two decades prior to its banning [2]. PCBs
are long lasting chemicals due to their sedimentation in the soil and resistance
to degradation [2]. They cause serious health issues in animals exposed to them,
such as cancer, through their stimulation of the aryl hydrocarbon receptor (AHR),
which is an important transcription factor [2]. PCBs bind to the AHR forming an
active AHR-ligand complex that enters the nucleus and activates genes at the
wrong time [2]. The most studied AHR is AHR2 due to it being the most active
version in fish species [4].
The
presence of PCBs in the Hudson River created a strong selection force against Atlantic
tomcod expressing the normal AHR. This strong selection force combined with
genetic mutation resulted in alleles expressing some form of PCB resistance to
be favored, as individuals with PCB resistant phenotypes are capable of surviving
and reproducing in this toxic environment [1]. The adaption to high levels of
toxins takes on the form of an AHR2 that is two amino acids shorter than the AHR2
typically seen in fish, the result of a six base pair deletion [4]. This small change
gives the receptor a significantly lower affinity for PCBs, preventing them
from turning on genes that should not be activated [2][4].
 |
| Figure 1. Overview of PCB Resistance through AHR Mutation [2] |
Other
fish from less polluted waters would not survive in the Hudson River due to
them lacking the PCB resistant AHR. Take for instance the Atlantic tomcod
populations of the Connecticut Niantic River and Shinnecock Bay in Long Island.
In both of these populations the presence of this variant is small (~5%)
whereas the presence of the variant in the Hudson River population is extremely
high (99%), with the non-variant allele only observed in heterozygotes [4]. The
low presence of this AHR2 mutant in other fish populations indicates that this
variant is generally not favored, further confirming that the mutated AHR2
expressed in the Atlantic tomcod of the Hudson River was a result of fast
adaption (<60 years) to extremely high levels of toxins in its environment
[2].
While
the Atlantic tomcod possesses immunity to the toxic effects of PCBs, the same
cannot be said for the species higher up in the food chain as all species
experience change at a different pace. What results is the passing of PCBs present
in the fish to predators that may not possess resistance to PCBs. In such a
manner, the water pollution caused by toxins has consequences that extend beyond
its immediate effects on the Atlantic tomcod population. In an effort to reduce
the pollution, General Electric is currently in the process of dredging out the
contaminated sediment from the Hudson River [2][3]. As the mutated AHR is only
favored in this specific type of environment, it is possible that the removal
of the toxic chemicals will affect the fitness of the Atlantic tomcod of the
Hudson River, resulting in another shift in the evolutionary pattern of this
species.
-Mary
Morales
Word
Count: 639
References:
[1] Roy,
N.K., S.C. Courtenay, R.C. Chambers, I.I. Wirgin. 2006. Characterization of the aryl
hydrocarbon receptor repressor and a comparison of its expression in Atlantic
tomcod from resistant and sensitive populations. Environmental Toxicology and Chemistry 25: 560-571.
[2] “Toxic
River means rapid evolution for one fish species.” 2011. Understanding Evolution. Web. <http://evolution.berkeley.edu/evolibrary/news/110301_pcbresistantcod>.
[4]
Wirgin, I., N.K. Roy, M. Loftus, R.C. Chambers, D.G. Franks, M.E. Hahn. 2011. Mechanistic
Basis of Resistance to PCBs in Atlantic Tomcod from the Hudson River. Science 331: 1322-1324
Was any research done on the possible effects of being a carrier for the mutated AHR allele (i.e. heterozygote advantage)? Also, how long do you think it will take General Electric to remove the contaminants?
ReplyDeleteWhat are the possible tradeoffs for having a mutated aryl hydrocarbon receptor (AHR)that makes it only selectively advantageous in an environment with high PCBs levels?
ReplyDeleteDoes the PCB-resistance mutation confer any phenotypic advantages or disadvantages? Because an 18 base pair deletion (coding for the 6 amino acids) sounds like a very significant nonsynonymous mutation.
ReplyDeleteWhat genes does AHR target? Are they different depending on the age of the fish or where it is in development?
ReplyDeleteI could see how the presence of PCB acted as an artificial selection force on the exposed animals. Since the dumping of this chemical is banned now, is there less frequency of PCB-resistant genes?
ReplyDeleteHow is the water affected by the presence of PCB? You mention how the company is attempting to remove contaminated sediments, but is that truly enough? I agree with Peter's comment about changes in allele frequencies. If the contamination level decreases significantly, would it matter if the fish kept the resistance, or would they begin to lose it?
ReplyDeleteWow, it's really interesting that these PCB-resisting mutations are driving evolution of the tomcod population as a whole. Say that the PCB-resistant AHR variant was not present in the population at all-- how do you think the influx of toxins into the river would affect the tomcod population? In other words, do you think that the presence of this PCB-resistant AHR mutation effectively saved the tomcod population, or do you think that the PCB's wouldn't have had that significant of an impact on a population containing all normal AHR genes?
ReplyDeleteThis is an important article to share. I cannot emphasis how bad water pollution is to many other species that depend on water bodies in one way or another. I am aware that another pollutant, methylmercury, actually causes certain bird species, such as American White Ibis, to exhibit homosexual behavior.
ReplyDelete